Wednesday, June 3, 2009

Beta blockers: good idea or trap?

For a few months in 2007 I worked very hard at bugging doctors to try to figure out what was going wrong. (A year later I tracked it to a problem with cholinesterase inhibitors, but I didn't know that then.) A neurologist I saw once (and only once) as part of this quest expressed that I was just being overly sensitive and suggested I try beta blockers.

When beta 1 receptors bind to epinephrine they make your heart beat harder and faster. This is what gives you that fluttery messed up feeling when you have to do something like get up and perform in front of a group of people. Beta blockers suppress, or at least attenuate, this effect. They're sometimes used (or abused, depending on your viewpoint) to control physiological symptoms of performance anxiety. This was the basis of his suggestion. Sounds like a good thing, right?

The problem is this: most neurons will adjust their gains and receptor densities to maintain a fairly constant level of input. This is a big part what goes on with things like drug tolerance. In this case, it means that while you're on beta blockers your beta receptors proliferate and ramp their gains to max trying desperately to get the signal level they expect. While the beta blocker levels are stable you feel fine, but when it goes down -- oh man...

I really wish they'd warned me about this when they suggested and/or prescribed the &%^$ things, but I learned this the hard way. I had to stop taking them for a while to do a test. The day after I stopped I felt jumpy, my heart rate was running ~130 just sitting still and ~160-180 if I tried to do anything, and I got really bad cardiac arrhythmia (multiple times per minute -- scary). This was not fun and so, so much worse than what had been happening to me before taking the beta blockers.

I tried to go without them after that, figuring these symptoms would fade and that I'd already paid the worst of the withdrawal symptoms waiting for the stupid test to happen. Months later, when these problems were still much worse than they'd been before and weren't getting any better I gave in and started taking them again. (BTW, the lovely interlude with the generic Ethex Toprol XL described in the last post happened at this point in the story.)

A few months after changing my diet to avoid cholinesterase inhibitors, I started having a different problem: the beta blockers were now too strong. The built up SGA had been keeping the epinephrine level artificially high. Once the level dropped enough, the beta blockers were making my blood pressure go so low I couldn't function.

I was already taking the minimum available dosage. Cutting them in half worked for a few weeks, but they couldn't be subdivided further without destroying the time release. (As described in the last post smooth time release is critical for this stuff.) The only option was go cold turkey and be miserably jumpy, heart racy, and arrhythmic until the beta receptors desensitized back to normal.

I couldn't find any useful info anywhere to help me understand how long that might take. The last experience stopping beta blockers was miserable and ultimately failed, but how much of that was caused by the hypersensitive beta receptors and how much by the high SGA levels?

It wasn't nearly as bad as I'd feared, implying that the SGA levels had been the dominant part of the problem last time. There was a little arryhthmia, but mild, and only for a few days. The jumpiness and heart racing faded slowly over a couple months.

Later, when I got the results back from 23andme, I discovered that I have mutant beta 1 receptors: GG on rs1801252. Only ~4% of the population have this genotype, and it's been associated with "low extroversion." I take that to mean that we suffer the fluttery feeling so bad that we mostly avoid having to be on stage in the first place. This may help explain why the beta blockers were so effective at such low doses.

So, the question is this: should I recommend the use of beta blockers to help counteract the effects of cholinesterase inhibitor sensitivity (CIS) during the detoxification process or not? It helped in the short term, but in the end felt like a trap. Also, I don't know how the mutant receptors play into this. How would this play out in people with CIS but with normal receptors? Sigh, need bigger sample size.

The more troubling thing is that ~millions of people are taking beta blockers for high blood pressure. It seems like everyone I talk to over the age of 60 is either taking them, or their spouses or friends are. Nobody warned them about receptor sensitization and withdrawal effects either. Yikes...

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